Fig. 2. Mutations in hop or mrl do not enhance Draf or Ras1 mutant phenotypes. (A) In mrl GLC embryos, the size of the posterior tll expression domain appears similar to wild type. (B) hop or mrl GLC embryos have identical phenotypes (mrl⁶³⁴⁶ mutant is shown) with a characteristic deletion of A5. (C) The tll expression pattern in hop^C111 Draf^C110 GLC embryos is indistinguishable from that in Draf^C110 GLC embryos. (D) These embryos exhibit cuticle phenotypes that resemble those of hop^C111 embryos. (E) The size of the posterior tll expression domain in hop^C111 Draf^PB26 double GLC embryos is similar to that of Draf^PB26 GLC embryos. (F) The cuticles of these embryos exhibit defects of both hop^C111 and Draf^PB26 mutants. (G) 19% of the Ras1^C40B mrl⁶³⁴⁶ double mutant embryos (n=18/97) have residual posterior tll expression that is similar to Ras1^C40B GLC embryos. (H) The cuticle defects of the Ras1^C40B mrl⁶³⁴⁶ double GLC embryos are a combination of those associated with Ras1^C40B and mrl⁶³⁴⁶ mutants, respectively, i.e., they show characteristic deletion of A4 and A5 due to the mrl⁶³⁴⁶ mutation and defects in posterior structures similar to Ras1^C40B and mrl⁶³⁴⁶ GLC embryos.

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